A properly functioning human heart maintains its own intrinsic rhythm, and is capable of pumping adequate blood throughout the body's circulatory system. However, some people have irregular cardiac rhythms, referred to as cardiac arrhythmias. Such arrhythmias can result in diminished blood circulation. To treat such arrhythmias, cardiac stimulation devices can be implanted in a patient and used to deliver therapy to the patient's heart.
Such implantable stimulation devices can include pacemakers and/or defibrillators. Pacemakers deliver timed sequences of low energy electrical stimuli, called pace pulses, to the heart, such as via an intravascular leadwire or catheter (referred to as a “lead”) having one or more electrodes disposed in or about the heart. Heart contractions are initiated in response to such pace pulses (this is referred to as “capturing” the heart). By properly timing the delivery of pace pulses, the heart can be induced to contract in proper rhythm, greatly improving its efficiency as a pump. Pacemakers can be used, e.g., to treat patients with bradyarrhythmias, where a heart beats too slowly, or irregularly.
Defibrillators deliver higher energy electrical stimuli to the heart. Defibrillators can include cardioverters, which synchronize the delivery of the high energy electrical stimuli to portions of sensed intrinsic heart activity signals. Defibrillators can be used, e.g., to treat tachyarrhythmias, that is, where a hearts beat too quickly.
Tachyarrhythmias can cause diminished blood circulation because the heart doesn't have sufficient time to fill with blood before contracting to expel the blood. A defibrillator is capable of delivering a high energy electrical stimulus (often referred to as a shock), which interrupts the tachyarrhythmia, to thereby allow the heart to reestablish a normal sinus rhythm for the efficient pumping of blood.
Ventricular tachyarrhythmias, which originate in the ventricles, include ventricular tachycardia (VT) and ventricular fibrillation (VF). Ventricular arrhythmias are often associated with rapid and/or chaotic ventricular rhythms. For example, sustained ventricular tachycardia can lead to ventricular fibrillation. In sustained ventricular tachycardia, consecutive impulses arise from the ventricles at a rate of 100 bpm or more. Such activity may degenerate further into disorganized electrical activity known as ventricular fibrillation (VF). In VF, disorganized action potentials can cause the myocardium to quiver rather than contract. Such chaotic quivering can greatly reduce the heart's pumping ability. Indeed, approximately two-thirds of all deaths from arrhythmia are caused by VF. A variety of conditions such as, but not limited to, hypoxia, ischemia, pharmacologic therapy, and asynchronous pacing may promote onset of ventricular arrhythmia. VF is typically fatal if not corrected within minutes.
A ventricular defibrillation threshold (VDFT) is the smallest amount of energy that can be delivered to the heart to reliably convert a ventricular fibrillation (VF) to a normal sinus rhythm. VDFTs vary from patient to patient, and may even vary within a patient depending on the placement of the electrodes used to deliver the therapy. In order to ensure the efficacy of such therapy and check device system integrity, the defibrillation threshold is preferably determined to ensure there is a large enough safety margin between the VDFT and a device's maximum shock capability. A large safety margin could prevent shock failure in case of increased VDFT caused by disease progression or the side effects of medication therapy. Determining VDFT could also provide information so that the defibrillation energy can be safely set above the threshold value but not at the device maximum capability, which might prolong device longevity and reduce the risk of fatal electro-mechanical dissociation caused by high energy shock.
Conventional techniques for determining VDFTs induce targeted tachyarrhythmias (e.g., ventricular fibrillations), and apply shocks of varying magnitude to determine the energy needed to convert arrhythmias into normal heart rhythms. However, such shocks can cause myocardial injury and hemodynamic instabilities. Further, such shocks are typically painful to the patient.
Since such conventional VDFT determination techniques subject patients to multiple VF episodes and high voltage shocks, exposing them to potentially detrimental effects of VF and applied shock, a patient's VDFT is often not determined. Alternatively, some physicians, mainly electrophysiologists, have used what is referred to as an abbreviated defibrillation safety margin (DSM) test, instead of the conventional VDFT test. However, with this abbreviated safety margin test, there is less certainty about the defibrillation efficacy of the selected shock strength.
A technique for estimating a patient's VDFT without applying defibrillation shocks or subjecting a patient to defibrillation has been proposed in U.S. Pat. No. 6,859,664, entitled “Cardiac Rhythm Management System with Defibrillation Threshold Prediction” (Daum et al.), which is incorporated herein by reference. In such technique, very low strength stimulation pulses (of less than 10 millijoules) are delivered to the patient's right ventricle (RV) using an RV coil electrode. A response is then measured between the RV coil electrode and an RV tip electrode, and between the RV tip electrode and the device housing, to thereby estimate the electric field distribution near the RV shock coil electrode. A distance from the RV shock electrode to the outer periphery of the left ventricular (LV) apex is also measured, e.g., using a fluoroscope or other imaging apparatus. Then, based on the estimate the electric field magnitude (also referred to as “potential gradient”) near the RV shock electrode, and the measured distance from the RV shock electrode to the outer periphery of the left ventricular (LV) apex, a VDFT is estimated using a model of electric field distribution that provides a desired electric field magnitude (e.g., 5 Volts/cm) throughout the heart, including at its periphery.
While the VDFT estimation technique of the '664 patent does not subject a patient to fibrillation or high energy shocks, the inventors of the present invention question its accuracy. More specifically, the VDFT estimation of the '664 patent use potential gradient measurements in the RV, generalized potential gradient from passive electric field model, and distance measurements, to extrapolate what stimulation levels would be necessary to achieve a desired potential gradient (e.g., 5 Volts/cm) at the left ventricle (LV) epicardial surface near the apex, which is the least affected region in conventional transvenous defibrillation configuration. Such approximations introduce errors because they ignore another determinant of voltage gradient—the heterogeneity of cardiac tissue resistivity. Such errors can be significant in a diseased heart having malignant structural and functional heterogeneities. Moreover, the stimulations levels (≦10 V) used in the '664 patent are very far away from the actual voltage range of VDFT (150˜830 V). Thus, the extrapolation of the '664 patent that uses passive models and relatively low stimulation levels may not be accurate enough to predict the VDFT.
Accordingly, there is a need for new techniques for estimating VDFTs. Preferably such techniques do not require the induction of ventricular fibrillation episodes.